A General Unfolding Speech Enhancement Method Motivated by Taylor's Theorem

While deep neural networks have facilitated significant advancements in the field of speech enhancement, most existing methods are developed following either empirical or relatively blind criteria, lacking adequate guidelines in pipeline design. Inspired by Taylor's theorem, we propose a general unfolding framework for both single- and multi-channel speech enhancement tasks. Concretely, we formulate the complex spectrum recovery into the spectral magnitude mapping in the neighborhood space of the noisy mixture, in which an unknown sparse term is introduced and applied for phase modification in advance. Based on that, the mapping function is decomposed into the superimposition of the 0th-order and high-order polynomials in Taylor's series, where the former coarsely removes the interference in the magnitude domain and the latter progressively complements the remaining spectral detail in the complex spectrum domain. In addition, we study the relation between adjacent order terms and reveal that each high-order term can be recursively estimated with its lower-order term, and each high-order term is then proposed to evaluate using a surrogate function with trainable weights so that the whole system can be trained in an end-to-end manner. Given that the proposed framework is devised based on Taylor's theorem, it possesses improved internal flexibility. Extensive experiments are conducted on WSJ0-SI84, DNS-Challenge, Voicebank+Demand, spatialized Librispeech, and L3DAS22 multi-channel speech enhancement challenge datasets. Quantitative results show that the proposed approach yields competitive performance over existing top-performing approaches in terms of multiple objective metrics.Comment: Submitted to TASLP, revised version, 17 page

DMF-Net: A decoupling-style multi-band fusion model for full-band speech enhancement

For the difficulty and large computational complexity of modeling more frequency bands, full-band speech enhancement based on deep neural networks is still challenging. Previous studies usually adopt compressed full-band speech features in Bark and ERB scale with relatively low frequency resolution, leading to degraded performance, especially in the high-frequency region. In this paper, we propose a decoupling-style multi-band fusion model to perform full-band speech denoising and dereverberation. Instead of optimizing the full-band speech by a single network structure, we decompose the full-band target into multi sub-band speech features and then employ a multi-stage chain optimization strategy to estimate clean spectrum stage by stage. Specifically, the low- (0-8 kHz), middle- (8-16 kHz), and high-frequency (16-24 kHz) regions are mapped by three separate sub-networks and are then fused to obtain the full-band clean target STFT spectrum. Comprehensive experiments on two public datasets demonstrate that the proposed method outperforms previous advanced systems and yields promising performance in terms of speech quality and intelligibility in real complex scenarios

Alternative splicing in the variable domain of CaMKIIβ affects the level of F-actin association in developing neurons.

The Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) β has an essential function in dendritic spines via binding to and reorganization of the actin cytoskeleton during plasticity events not shared by CaMKIIα isoform. CaMKIIβ and CaMKIIα isoforms have remarkable structural differences within the variable region. Three exons (E1, E3, and E4) are present in CaMKIIβ but not in CaMKIIα gene. Four splice variants of CaMKIIβ isoforms (CaMKIIβ, β\u27, βe and β\u27e) were discovered in embryonic and adult brains. Exons E1 (lacked in βe and β\u27e) and E4 (lacked in β\u27 and β\u27e) are subject to differential alternative splicing. We hypothesized that the sequences encoded by exons E1, E3, and/or E4 are involved in CaMKIIβ-specific bundling to the F-actin cytoskeleton. We tested the colocalization and association of these CaMKIIβ variants within an F-actin-rich structure (microspike) in CaMKIIα free embryonic day 18 (E-18) rat cortical neurons. Our results showed that CaMKIIβ and CaMKIIβ\u27 containing exon E1 displayed an association with F-actin, while CaMKIIβe and CaMKIIβ\u27e lacking E1 did not. Moreover, CaMKIIβ\u27 lacking exon E4 but having E1 showed decreased actin bindingcapacity compared to WT CaMKIIβ. This suggested E1 is required for the association between CaMKIIβ and F-actin, while E4 assists CaMKIIβ to associate with F-actin better. Thus, alternative splicing of CaMKIIβ variants in developing neurons may serve as a developmental switch for actin cytoskeleton-associated isoforms and therefore correlated with dendritic arborization and synapse formation during LTP